Study Finds Protein Tied to Colon Cancer Onset and Progression

U.S., Dec. 13 -- A recent study led by a team of researchers at the Comprehensive Cancer Center at St. Jude Children's Research Hospital has established that a model system may help scrutinizing the process by the means of which a protein that is often mutated in human cancer exerts its tumor-silencing effects.
Cancers are caused by direct alterations in the genetic code but some cancers can also arise from epigenetic events that influence gene expression in other ways. The investigators demonstrated that ARID1A - a component of the SWI/SNF chromatin remodeling complex - serves as a tumor suppressor in the colon but not in the small intestine of mice.
The experts discovered that enhancers, which are the short regions of DNA that specify which genes are activated in each cell type, were a significant part of the interaction between ARID1A and the SWI/SNF chromatin remodeling complex.
The researchers showed that the loss of ARID1A impairs control of cell recognition in the colon and promotes cancer formation. The novel results clarify how epigenetic processes play a role in gene regulation and the beginning of colon cancer.
The study was published in the journal Nature Genetics.